Recent research indicates that the metabolic syndrome develops during childhood and is associated with several early risk factors including low (<= 10th percentile body mass index [BMI-USCDC]) or high (>= 90th percentile [BMI-USCDC]) birth weight. However, markers that precede the syndrome and mechanisms that explain these relationships have yet to be identified. These mechanisms may originate in the intrauterine environment, be exacerbated in susceptible populations, such as African Americans and, be further promoted by an early "obesigenic" environment. Thus, we propose that young African American children with low or high birth weight may be predisposed genetically and behaviorally to the early manifestation of subtle, non-symptomatic metabolic abnormalities that work synergistically to create a metabolic syndrome phenotype. The metabolic abnormalities increasing the propensity to type 2 diabetes may originate earlier than previously proposed. In adults insulin sensitivity is correlated negatively with lipid depots in the skeletal muscle (intramyocellular lipids = IMCL) and in the liver long before the development of diabetes. Noninvasive techniques for examining the relationship of skeletal muscle and liver lipids to insulin sensitivity have not been applied to prepubertal African American youth. How early and to what extent metabolic abnormalities occur in children and whether it is more prevalent in African American vs. Caucasian children are unknown. We therefore propose to: 1) Explore the potential markers and mechanisms of impaired insulin sensitivity in pre-pubertal (7-9 years) African American and Caucasian children with low or high birth weight. 2) Determine the relationship of birth weight and ethnicity to insulin sensitivity in these youth. We aim to explore potential markers and mechanisms of the impaired insulin sensitivity observed in 7-9 y prepubertal children by examining the relationships between insulin sensitivity and ectopic fat deposition i.e. triglyceride content in skeletal muscle and liver, abdominal fat (independent of ectopic fat), resting energy metabolism (REE and respiratory quotient [RQ] [fat oxidation] and cardiovascular disease risk factors lipid profiles and blood pressure). Insulin Sensitivity will be measured by Frequently Sampled Intravenous Glucose Tolerance Test (FSIGTT), triglyceride contents in skeletal muscle and liver by Nuclear Magnetic Resonance pectroscopy (ill-MRS) and energy metabolism by ventilated hood indirect calorimetry. A secondary aim is to examine he relationship of birth weight and ethnicity (African American vs. Caucasian) to insulin sensitivity in children, 7-9 years (with and without adjusting for total body fat and/or ectopic fat).